Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_40_библиотеки_им_акад_М_И_Перельмана
.pdf
198
https://t.me/medicina_free
CHAPTER 7 | INFLAMMATORY BOWEL DISEASE AND COLONICDISORDERS
35. E. Short- chain fatty acid enemas (SCFAs)
• Diversion colitis may occur early or late post- defunctioning
• Of those with histological evidence, only up to one third have symptoms
• Treatment may involve SCFA enemas, corticosteroid, or mesalazine enemas. Restoration of
gut continuity is the only denitive treatment.
The diagnosis of diversion colitis can occur within a few months or after three years following
defunctioning. The majority of patients have histological evidence, but it is not mandatory for the
diagnosis. Of those with histological evidence, only up to one third have symptoms. Symptoms may
include tenesmus, anorectal pain, mucous discharge, and rectal bleeding.
Diversion colitis is thought to occur as a result of deciency of SCFAs. Unabsorbed carbohydrates
entering the colon are metabolized by bacteria to SCFAs, such as butyric acid, that provide
nutrition for the colonic mucosa. Butyrate is an oxidative substrate for colonocytes. Evidence
suggests that SCFAs relax vascular smooth muscle and their deciencies may result in a relative
ischaemia to colorectal mucosa. Diversion colitis may therefore respond to SCFA enema treatment.
Corticosteroid enemas and mesalazine may also have a role. Treatment is not urgent because many
cases resolve spontaneously.
This patient has quiescent CD. Therefore, medical therapy is not indicated. Surgical options should
also be considered. Restoration of continuity and faecal stream provides denitive treatment.
Tominaga K, Kamimura K etal. Diversion colitis and pouchitis:a mini- review. World J Gastroenterol.
208;24(6):734– 747. Doi:0.3748/ wjg.v24.i6.734.
36. D. Preservation of crypt architecture
• Right- sided and transverse colon biopsies give the highest diagnostic yield in microscopic colitis
• An increase in the colonic mucosal subepithelial collagen layer is indicative of collagenous
colitis
• Treatment with budesonide is eective although a third may relapse
Microscopic colitis can be divided into two subgroups— collagenous and lymphocytic colitis.
Presentation is with watery, secretory, non- bloody diarrhoea. Onset can be sudden or gradual.
Medications including proton pump inhibitors (PPIs), NSAIDs, and Selective Serotonin Reuptake
Inhibitor (SSRIs) are common causes. Forty per cent of patients may have concomitant autoimmune
disease such as coeliac disease or thyroid dysfunction.
Diagnosis is based on histology. Macroscopic ndings at colonoscopy will be normal. Pancolonic
biopsies need to be taken because there is a signicant false- negative rate (40%) if only the left
colon is biopsied. Right- sided and transverse colon biopsies give the highest yield.
Histologicalndings
• Collagenous colitis:
• Intact crypt architecture
• Increase in the colonic mucosal subepithelial collagen layer
• Acollagen band >10 µm thick, usually type Ior III collagen, rather than type IV (normal
measurement 2– 5 µm)
• Lymphocytic colitis:
• Increased numbers of intraepithelial lymphocytes
• Absence of increased subepithelial collagen layer
• >20 lymphocytes per 100 epithelial cells
CHAPTER 7 | ANSWERS
https://t.me/medicina_free
199
By contrast, the histological lymphocyte count in normal, IBD, and infectious colitis specimens is
4– 5 lymphocytes per 100 epithelial cells.
Management includes removal of oending medication, whenever possible, and investigation for coexistent coeliac disease. For mild symptoms, anti- diarrhoeal agents such as loperamide can be used
rst and, if symptoms are severe, a course of budesonide may help. However, if corticosteroids
are ineective, other therapies such as 5- ASAs and thiopurines may be required. The patient can
be reassured that, although relapse may occur, there is no association with the development of
malignancy:colonoscopic surveillance is not necessary.
Boland K, Nguyen G.Microscopic colitis:a review of collagenous and lymphocytic colitis. Gastroenterol
Hepatol (N Y). 207 Nov;3():67– 677. PMID:2923046.
37. E. 96%
• Glutamate dehydrogenase (GDH) antigen testing is a rapid screening tool that determines
whether a patient is colonized with Clostridioides dicile or not
Clostridioides dicile (C.dicile) is a gram- positive bacillus that colonizes the gut following
transmission via the faecal– oral route and disruption of the gut ora, usually following a course of
antibiotics. There is a relatively high carrier population, especially in hospitals and care institutions.
The organism produces two exotoxins— toxin A(enterotoxin) and toxin B (cytotoxin). These are
responsible for the colonic inammation leading to diarrhoea and potentially pseudomembranous
colitis. Certain strains may not produce toxin A, leading to false- negative results.
In clinical practice, several dierent laboratory tests are available to diagnose C. dicile. Dierent
laboratory tests are often used in combination to conrm the diagnosis.
Glutamate dehydrogenase (GDH) antigentesting
• GDH is an enzyme produced by all strains of C.dicile, whether toxin or non- toxin producing.
Arapid test that determines whether a patient is colonized or not, in view of its high negative
predictive value (98.4%– 100%), it serves as a rapid screening test. The overall sensitivity of the
GDH assay is 96%.
• Another initial screening test is the nucleic acid amplication test (NAAT); if either are positive,
further analysis can be performed.
Cytotoxintesting
• This can follow a positive GDH screening test to determine whether or not the strain of
C.dicile is toxin producing. This can be done by means of the following:
• Cell culture cytotoxicity assay:High sensitivity although it is expensive and time consuming. If
positive, however, it does not require a second conrmatory test.
• Enzyme immunoassay (EIA):Detect toxins Aand B.It is quicker and simpler than the
cytotoxin assay, but has a higher rate of false negatives.
• Polymerase chain reaction: Rapid test with high sensitivity and specicity.
Anaerobic faecalculture
• This is not routinely used:it takes a long time to obtain results, and it does not dierentiate
between toxin- and non- toxin- producing strains.
A positive cell- culture cytotoxin assay as a stand- alone test can conrm the diagnosis.
Guery B, Galperine T etal. Clostridioides dicile:diagnosis and treatments. BMJ. 209
Aug;20;366:l4609. Doi:0.36/ bmj.l4609.
200
https://t.me/medicina_free
CHAPTER 7 | INFLAMMATORY BOWEL DISEASE AND COLONICDISORDERS
38. C. Ivermectin
• Peripheral blood eosinophilia is indicative of strongyloidiasis
• Larva currens— a migratory, pruritic rash is pathognomonic of chronic infection
• Unlike most intestinal helminth infections, strongyloidiasis can be chronic
This patient is suering from strongyloidiasis due to infection with the nematode, Strongyloides
stercoralis. Although common in the tropics or subtropics, S. stercoralis is also found in southern
Europe and the USA.
S. stercoralis infects humans through contact with soil containing the larvae. The life cycle of
S. stercoralis includes autoinfection via the gastrointestinal tract. Therefore, a state of chronic
strongyloidiasis can occur.
Infection with S. stercoralis may be asymptomatic (60%) or mild. Chronic infection may give a
pathognomonic rash described as ‘larva currens’— a creeping eruption caused by subcutaneous
migration of the larvae. It is raised and itchy like a wheal, transient, and usually develops on the
trunk of the body. Other symptoms of chronic strongyloidiasis include abdominal pain, intermittent
diarrhoea, weight loss, and rarely a dry cough or wheeze if the larvae migrate to the lungs.
Diagnosis is dicult. However, peripheral blood eosinophilia is indicative. Three stool samples for
microscopy and S. stercoralis serology should be sent from those with a compatible history. Faecal
microscopy has a low sensitivity (50%) due to intermittent larval excretion. However, it remains the
gold standard.
A rare complication of S. stercoralis is hyperinfection syndrome. This occurs when the chronically
infected patient becomes immunosuppressed. This triggers widespread dissemination of lariform
larvae into tissues, with the risk of bacterial infection as they migrate through the bowel wall.
Features may include bloody diarrhoea, bowel perforation, gram- negative septicaemia, pulmonary
exudates, or meningoencephalitis.
Treatment is with anti- helminth agents (such as ivermectin) and supportive therapy.
Greaves D, Coggle S etal. Strongyloides stercoralis infection. BMJ. 203;347. Doi:0.36/ bmj.f460.
39. A. Campylobacter jejuni
• Campylobacter is the most common bacterial cause of acute gastroenteritis in Europe
• It typically causes one week of fevers, diarrhoea +/– blood and signicant abdominal pain
• Campylobacter infection is typically self- limiting although antibiotics have a modest impact on
duration of symptoms and may be used in severe cases
In Europe, Campylobacter has been the most commonly reported gastrointestinal bacterial
pathogen over the past 10years. This is followed by infection with Salmonella, C dicile, Shiga-
toxin/ verocytotoxin- producing Escherichia coli (STEC/ VTEC) and Shigella. Contact with
contaminated poultry meat accounts for 80% of cases. Incubation period is three days and acute
illness is characterized by seven days of cramping, periumbilical abdominal pain, which may
mimic appendicitis, and diarrhoea. Bloody stools are observed in 15% of patients. Late onset
complications following Campylobacter infection include reactive arthritis (2%) and Guillain- Barré
syndrome (0.1%).
Most Campylobacter infections are self- limiting requiring supportive management alone. Antibiotics
shorten the duration of intestinal symptoms by 1.3days. However, because of their limited ecacy
and antimicrobial resistance, their use should be limited to those with, or at risk of, severe disease
(e.g. elderly or immunosuppressed patients). Norovirus is the most common cause of infectious
intestinal disease overall, and has a shorter disease course of two days with non- bloody diarrhoea
CHAPTER 7 | ANSWERS
https://t.me/medicina_free
201
and vomiting. C dicile is relatively rare outside a healthcare setting with only 25% of cases
diagnosed in the community. Bloody diarrhoea is also uncommon in C dicile infection.
European Centre for Disease Prevention and Control. Campylobacteriosis. In:ECDC. Annual
epidemiological report for 206. Stockholm:ECDC; 208.
40. C. Intravenous ganciclovir
• Cytomegalovirus (CMV) colitis is a rare cause of diarrhoea in HIV- infected patients and CD4+
lymphocyte count <50 cells/ microlitre
• First line treatment of CMV colitis is with intravenous ganciclovir
CMV gastrointestinal disease is a serious complication of acquired immunodeciency syndrome
(AIDS), occurring at CD4+ <50 cells/ microlitre, and it has fortunately become rare in the era of
potent antiretroviral therapy (ART). Most clinical disease occurs in individuals previously infected
with CMV and represents re- activation of latent infection. CMV colitis is characterized by lowgrade fever, weight loss, anorexia, abdominal pain, and debilitating diarrhea. Haemorrhage and
perforation can be life- threatening complications. Mucosal ulceration is seen at endoscopy and
characteristic intranuclear and intracytoplasmic inclusions are found in histology samples. Most
heavily immunosuppressed patients will have positive CMV serology that does not indicate endorgan involvement. Intravenous ganciclovir is the rst- line treatment for CMV colitis that can
be converted to oral valganciclovir to allow outpatient management typically for 3– 6 weeks.
Intravenous foscarnet has a signicant side eect prole (renal impairment and seizures) but can
be used as second- line therapy in cases of ganciclovir toxicity (myelosuppression) or resistance.
ART should also be introduced. However, those with comorbid CMV retinitis should receive two
weeks of CMV treatment prior to ART to reduce the risk of intraocular inammation secondary to
immune reconstitution. Cryptosporidiosis and disseminated mycobacterium avium complex disease
are both causes of diarrhoea in HIV- infected patients, and can be treated with nitazoxanide and
clarithromycin plus ethambutol respectively.
Yerushalmy- Feler A, Padlipsky J, Cohen S.Diagnosis and management of CMV colitis. Curr Infect Dis
Rep. 209 Feb 5;2(2):5. Doi:0.007/ s908- 09- 0664- y.
41. E. No surveillance
• Colonoscopic surveillance is not indicated in patients not meeting criteria for high- risk features
at baseline colonoscopy
• The average lead time for progression of an adenoma to cancer is 10years
• No surveillance is recommended if life expectancy is less than 10years or if patient is older
than 75years
For further information on this subject, please refer to gure1 from the British Society of
Gastroenterology, the Association of Coloproctology of Great Britain and Ireland and Public Health
England published consensus guidelines in 2019 regarding surveillance following adenoma removal.
You can nd the article in full here:https:// www.bsg.org.uk/ wp- content/ uploads/ 2019/ 09/ 201.
full_ .pdf
Rutter MD, East J et al. BSG/SCPGBI/PHE Post-polypectomy and post-colorectal cancer resection
surveillance guidelines. Gut 2020;69(2):20–223. Doi:0.36/gutjnl-209-39858.
202
https://t.me/medicina_free
CHAPTER 7 | INFLAMMATORY BOWEL DISEASE AND COLONICDISORDERS
42. B. Three- yearly colonoscopy
Patients with acromegaly:
• These patients are at increased risk of developing CRC
• Specic colorectal screening is required, which diers from other CRC screening programmes
• Colonoscopic screening should start at the age of 40years (unless there are colonic symptoms
at an earlier age)
• If an adenoma is found at rst screening, or serum insulin- like growth factor- 1 levels are
elevated above the maximum of the age- corrected normal range, colonoscopic screening
should be oered three- yearly
• If the initial colonoscopy is negative, or hyperplastic polyps are found, or the growth
hormone/ insulin- like growth factor- 1 levels are normal, screening should be oered every
5– 10years
• Colonoscopy is required, rather than sigmoidoscopy, because a signicant number of
adenomas and carcinomas are right- sided
• Colonoscopy can be technically more dicult because of the increased bowel length, loop
complexity, and poor bowel preparation. This can lead to a higher number of complications,
and patients need to be counselled about this
Cairns SR, Scholeeld JH, Steele RJ etal. Guidelines for colorectal cancer screening and surveillance
in moderate and high risk groups (update from 2002). Gut. 200;59(5):666– 689. Doi:0.36/
gut.2009.79804.
43. D. MUTYH- associated polyposis (MAP)
• MAP is an autosomal recessive condition
• Colorectal surveillance should commence at 18– 20years old; if surgery is not undertaken,
then annual surveillance is recommended
• Upper GI surveillance should be considered at 35years old
All except MAP are due to dominant transmission of a gene defect associated with a susceptibility
to CRC and other cancer types.
• The MutY human homologue (MYH) gene is located on chromosome 1p and is one of three
identied genes involved in base- excision repair
• MYH, discovered in 2002, encodes for MUTYH glycosylase, which is involved in oxidative
DNA damage repair
• MAP is inherited in an autosomal- recessive pattern.
• It accounts for less than 0.4%– 3% of all CRCs; the population prevalence of heterozygotes
is 1:100
• The lifetime risk of a homozygous person developing CRC is estimated to be 100% at 60years
• The number of colonic polyps found in MAP can vary signicantly from thousands to fewer
than 100
• CRC in MAP is more likely to be right sided and synchronous
• Upper gastrointestinal polyps have been seen, albeit rarely. The lifetime risk of developing
duodenal cancer is around 4%
• An increased incidence of breast cancer has been seen in female bi- allelic mutation carriers
• Heterozygotes may have a slightly increased risk of CRC compared with the general
population
CHAPTER 7 | ANSWERS
https://t.me/medicina_free
203
Management
• Colonoscopy surveillance should start at 18– 20years on an annual basis using dye- spray
colonoscopy for patients who are bi- allelic MUTYH carriers
• It is recommended that upper gastrointestinal surveillance is started at 35years old
• Depending on the number of polyps found and the degree of dysplasia, prophylactic
colectomy should be considered
• Breast screening should be considered because there may be an increased risk of developing
breast cancer
Monahan K, Dunlop M etal. Guidelines for the management of hereditary colorectal cancer from the
British Society of Gastroenterology (BSG)/ Association of Coloproctologists of Great Britain and Ireland
(ACPGBI)/ United Kingdom Cancer Genetics Group (UKCGG). Gut 2020;69(3):4–444.
Doi: 0.36/gutjnl-209-3995.
44. B. Colonoscopy and genetic testing for serine/ threonine kinase 11 gene mutation
• Peutz- Jeghers syndrome (PJS) is an autosomal dominant hamartomatous polyposis syndrome
• PJS is associated with a substantial risk of GI- related and breast cancers
• Surveillance by gastroscopy, colonoscopy, and video capsule endoscopy (VCE) should
commence at age eight years in asymptomatic patients with PJS
PJS is an autosomal dominant syndrome characterized by harmartomatous polyps in the GI tract
and mucocutaneous pigmentation of the lips, oral mucosa, and perianal region. Its prevalence is
between 1 in 8.300 and 1 in 29,000. The common germline mutation is STK11 (aka LKB1) located
on chromosome 19p. Approximately 40%– 80% of patients with PJS have no detectable pathogenic
mutation in STK11.
Diagnosticcriteria
This is based on any one of the following:
• ≥2 histologically conrmed PJ polyps
• Any number of PJ polyps detected in one individual who has a family history of PJS in a close
relative
• Characteristic mucocutaneous pigmentation in an individual who has a family history of PJS in
a close relative
• Any number of PJ polyps in an individual who also has characteristic mucocutaneous
pigmentation
• Apathogenic variant in STK11
Features such as hamartomatous polyps or characteristic mucocutaneous pigmentation should lead
to genetic evaluation. If PJS is conrmed, all FDRs should be tested.
In an asymptomatic patient with PJS, gastrointestinal surveillance by gastroscopy, colonoscopy, and
VCE commence at the age of eight years. We recommend that small bowel surveillance should
continue three yearly. If baseline colonoscopy and OGD are normal, then they can be safely
deferred until age 18years. However, if polyps are found at baseline examination, then they should
be repeated three yearly. Earlier investigation of the GI tract should be performed in symptomatic
patients.
Surveillance forPJS
PJS is associated with a substantial risk of colon, stomach, pancreatic, and breast cancers. However,
the malignant potential of the PJS polyp is unclear.
204
https://t.me/medicina_free
CHAPTER 7 | INFLAMMATORY BOWEL DISEASE AND COLONICDISORDERS
• In an asymptomatic patient, colonoscopy, gastroscopy, and VCE is indicated at eight years of
age. Small bowel surveillance should continue three yearly
• If baseline colonoscopy and OGD are normal, then they can be safely deferred until age
18years; however, if polyps are found at baseline examination, then they should be repeated
three yearly
• Earlier investigation of the GI tract should be performed in symptomatic patients
• Elective polypectomy to prevent polyp- related complications (e.g. intussusception, bleeding) is
recommended
Monahan K, Dunlop M etal. Guidelines for the management of hereditary colorectal cancer from the
British Society of Gastroenterology (BSG)/ Association of Coloproctologists of Great Britain and Ireland
(ACPGBI)/ United Kingdom Cancer Genetics Group (UKCGG). Gut 2020;69(3):4–444.
Doi: 0.36/gutjnl-209-3995.
45. A. One year
• Serrated polyposis syndrome (SPS) is diagnosed phenotypically
• Annual surveillance colonoscopy should be oered to all SPS patients until the colon has been
cleared of all lesions >5mm in size
• FDRs of patients with SPS should be oered an index colonoscopy at age 40years and veyearly surveillance thereafter dependent on polyp burden
This patient has SPS. Adiagnosis of SPS should be phenotypically driven because no single causative
gene has been identied. Individuals should full the phenotypic criteria as dened by the World
Health Organization in 2019 for a diagnosis of SPS to be made (Box 7.2).
Box 7.2 Updated World Health Organization clinical criteria forthe diagnosis ofserrated
polyposis2019
Criterion1
At least 5 serrated lesions/ polyps proximal to the rectum all being ≥ 5mm in size, with 2 or
more ≥ 10mm in size
Criterion2
More than 20 serrated lesions/ polyps of any size distributed throughout the large bowel, with
at least 5 proximal to the rectum
Note: Any histological subtype of serrated lesion/ polyp (hyperplastic polyp, sessile serrated lesion without or with dysplasia,
traditional serrated adenoma, and unclassied serrated adenoma) is included in the nal polyp count. The polyp count is
cumulative over multiple colonoscopies.
The prevalence of SPS in the West is 1:3,000. However, this may be an underestimate because the
awareness of this condition continues to increase among clinicians. The overall lifetime risk of CRC
is approximately 7%– 10% with an increased risk in FDRs of patients with SPS. There is a degree
of phenotypic overlap with other intestinal polyposis syndromes (e.g. MAP, attenuated Familial
adenomatous polyposis [FAP]). If the patient is under 50 or there are multiple aected relatives or
dysplasia in the polyp, one should exclude other polyposis syndromes with gene panel testing prior
to making a denitive diagnosis of SPS.
Colonoscopic surveillance should be performed yearly once the colon has been cleared of all
lesions >5mm in size. If no polyps ≥10mm in size are identied at subsequent surveillance
examination, the interval can be extended to two yearly. FDRs of patients with SPS should be
CHAPTER 7 | ANSWERS
https://t.me/medicina_free
205
oered an index colonoscopy at age of 40years or 10years prior to the diagnosis of the index
case. Thereafter, surveillance examination should occur ve- yearly unless polyp burden dictates
earlier assessment.
Monahan K, Dunlop M etal. Guidelines for the management of hereditary colorectal cancer from the
British Society of Gastroenterology (BSG)/ Association of Coloproctologists of Great Britain and Ireland
(ACPGBI)/ United Kingdom Cancer Genetics Group (UKCGG). Gut 2020;69(3):4–444.
Doi: 0.36/gutjnl-209-3995.
46. A. Biofeedback therapy (BFT)
• BFT is superior to other treatment modalities for dyssynergic defecation
BFT is an instrument- based learning process:it employs equipment to record a patient’s bodily
activities and then provides feedback to the patient as a sensory (visual, auditory, or verbal)
response. It was rst used in chronic constipation due to dyssynergia defecation to rehabilitate
anorectal function.
BFT requires active engagement. Therefore, preserved cognition and motivation are prerequisites
to treatment. Sessions last approximately one hour and a typical course of BFT may include 5– 10
sessions.
BFT has been shown to be ecacious in reducing dyssynergia and laxative use in patients
with dyssynergic defecation. Other treatment modalities, listed below, have limited benet in
comparison.
Treatmentmodalities
• Avoiding constipating medications
• Increasing bre (optimal intake is 20– 30 g daily) and uid intake
• Exercise
• Timed toilet training
• Laxatives
• Myectomy of the anal sphincter helps only 10%– 30% of patients
• Using botulinum toxin injections to paralyse the anal sphincter muscle and reverse the anal
spasm shows no improvement
In constipation that is refractory to medical therapy, surgery can be an option, including colectomy,
ileostomy, or ileorectal anastomosis.
Narayanan S, Bharucha A.Apractical guide to biofeedback therapy for pelvic oor disorders. Curr
Gastroenterol Rep. 209 Apr 23;2(5):2. Doi:0.007/ s894- 09- 0688- 3.
47. D. Prucalopride
• Prucalopride is a selective 5- hydroxytryptamine type 4 receptor (5- HT4) agonist
• Its use is licensed for women with chronic constipation in whom at least two dierent classes
of laxatives, at the highest tolerated dose for minimum 6months, have failed to be eective
Prucalopride is an 5- HT4 agonist:it has a stimulating eect on colonic motility. Transit studies show
that prucalopride increases gastric emptying, and small bowel and colonic transit.
Robust evidence has demonstrated the ecacy of prucalopride in severe constipation. Three large,
randomized controlled Phase III trials showed a signicant improvement in bowel function in up to
69% of patients treated over three months.
206
https://t.me/medicina_free
CHAPTER 7 | INFLAMMATORY BOWEL DISEASE AND COLONICDISORDERS
Its use is recommended for the treatment of chronic constipation in women:
• who have been treated with at least two dierent classes of laxatives at the highest tolerated
dose for at least six months
• in whom current treatment has failed to provide adequate relief
• for whom invasive treatment for constipation is being considered
If it is not eective after four weeks, appraisal of continued use should be considered.
The most common side eects are headaches, abdominal pain, nausea, and diarrhoea, and these
seem to be apparent early after starting treatment with prucalopride.
Tack J, Muller- Lissner S etal. Diagnosis and treatment of chronic constipation— a European perspective.
Neurogastroenterol Motil. 20 Aug;23(8):697– 70. Doi:0./ j.365- 2982.20.0709.x.
48. D. IBS
• FI is a common and unreported symptom
• IBS, diarrhoea, and prior cholecystectomy are the strongest independent risk factors for FI in
middle- aged women
‘Faecal incontinence’ is dened as any involuntary loss of faeces that causes a social or hygienic
problem. It is a common symptom that is often under- reported because of social stigma. Around
0.5%– 1.0% of adults suer from regular FI that aects their quality of life. Acommon error is to
assume that a single cause is responsible for a patient’s symptoms.
Baseline assessment includes:
• Taking a relevant medical and obstetric history
• Discussing the patient’s bowel habit
• Considering faecal loading or treatable causes of diarrhoea (e.g. IBD or IBS)
• Considering red ag symptoms for gastrointestinal cancer
• Performing a general examination and assessing for neurological sequalae of disc prolapse/
cauda equina syndrome
• Performing a rectal examination and assessing for rectal prolapse, third- degree haemorrhoids,
and anal sphincter injury, including obstetric and other trauma
• If appropriate, performing a cognitive assessment
According to a population- based case– control study conducted by the Mayo Clinic, diarrhoea, IBS,
and prior cholecystectomy are the strongest independent risk factors for FI in middle- aged women.
The mean age of onset of FI in this group was 55years. Less strong risk factors are a high BMI,
current smoking, rectocoele, and urinary stress incontinence. In contrast to being a risk factor for
postpartum FI, obstetric events on their own, such as vaginal delivery, forceps- assisted delivery, and
episiotomy, did not predict delayed FI.
Bharucha AE, Zinsmeister AR, Schleck CD etal. Bowel disturbances are the most important risk factors
for late- onset fecal incontinence:a population- based case– control study in women. Gastroenterology.
200;39:559– 566. Doi:0.053/ j.gastro.200.07.056.
49. C. Lipofuscin
• Melanosis coli is caused by chronic laxative use
• The pigment in melanosis coli is lipofuscin
• Melanosis coli is more common in the proximal colon
CHAPTER 7 | ANSWERS
https://t.me/medicina_free
207
The pigment in melanosis coli is lipofuscin, not melanin as the name may imply. Long- term use of
laxatives, typically from the anthranoid group, such as senna, cause melanosis coli. Anthraquinones
have a toxic eect on the epithelial cells of the colon; damage caused to intracellular components is
phagolysed. The products of this phagolysis are then found within the cells as lipofuscin. These cells
are phagocytosed by macrophages that can later be found in the mucosa and submucosa of the
colon. This commonly aects the proximal colon, which is thought to be related to the distribution
of macrophages in the colon. Melanosis coli may occur within a few months of chronic laxative
use. It is asymptomatic and often an incidental nding at colonoscopy. Treatment is cessation of
causative laxative.
Brown bowel syndrome is also a brown discoloration of the colon due to lipofuscin deposition.
Unlike melanosis coli, the lipofuscin deposits are found in the tunica muscularis but not in the
mucosa. An association between brown bowel syndrome, malabsorptive conditions, and vitamin E
deciency has been reported.
Aluminium, silicon, and magnesium are found in Peyer’s patches in melanosis ilei. Haemosiderin
in the lamina propria of the ileum has been found in a patient with melanosis ilei after chronic
ingestion of iron.
Nesheiwat Z, Al Nasser Y.Melanosis Coli. [Updated 2020 Jan5]. In:StatPearls [Internet]. Treasure
Island (FL):StatPearls Publishing; 2020 Jan. Available at:https:// www.ncbi.nlm.nih.gov/ books/
NBK49346/
50. D. Slow- transit constipation
• Presence of ≥6 markers in the colon on transit study is diagnostic of slow bowel transit
• Constipation is more common in women
• Secondary causes of constipation include drugs, and neurological and metabolic disorders
A colonic transit study measures whole gut transit time (primarily colon) via the ingestion of radioopaque markers. The study is inexpensive, simple, and safe. The patient ingests a single capsule
containing 24 markers on day 1, followed by a plain abdominal lm on day 6 (120 hours later).
In patients with normal transit time, fewer than 5 markers remain in the colon. The presence of
≥6 markers scattered throughout the colon is diagnostic of slow bowel transit. In dyssynergic
defecation, ≥6 markers are found in the rectosigmoid region, with near normal transit of markers
through the rest of the colon.
Primary or functionalconstipation
Constipation is common and polysymptomatic. The prevalence of chronic constipation ranges from
2% to 28%. Constipation is more common in women, with an estimated female:male ratio of 2.2:1.
Its prevalence increases with advancing age. Chronic constipation has a signicant impact on quality
of life and is a major cause of psychological distress.
Three subtypes of primary or functional constipation are known. However, overlaps exist.
• Slow- transit constipation is characterized by prolonged delay of the transit time of stool
throughout the colon
• Dyssynergic defecation (also known as ‘anismus’, ‘pelvic oor dyssynergia’, or ‘outlet
obstruction’) is diculty in expelling, or inability to expel, stool from the anorectum
• Irritable bowel syndrome with predominant constipation (IBS- C) is characterized by symptoms
of constipation, with discomfort or pain as a prominent feature
Соседние файлы в папке Библиотека им академика М.И. Перельмана